Alzheimer's & Dementia: The Journal of the Alzheimer's Association
Volume 4, Issue 1 , Pages 6-13, January 2008

Elevated microsomal prostaglandin-E synthase–1 in Alzheimer’s disease

  • Uzma A. Chaudhry

      Affiliations

    • Department of Anesthesiology/Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
  • ,
  • Hean Zhuang

      Affiliations

    • Department of Anesthesiology/Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
  • ,
  • Barbara J. Crain

      Affiliations

    • Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA
  • ,
  • Sylvain Doré

      Affiliations

    • Department of Anesthesiology/Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    • Corresponding Author InformationCorresponding author. Tel: 410-614-4859; Fax: 410-955-7271.

published online 14 December 2007.

Abstract 

Background

The proinflammatory prostaglandin E2 (PGE2) fluctuates over time in the cerebrospinal fluid of patients with Alzheimer’s disease (AD), but the cerebral distribution and expression patterns of microsomal prostaglandin-E synthase (mPGES)–1 have not been compared with those of normal human brains.

Methods

Middle frontal gyrus tissue from AD and age-matched control brains was analyzed by Western blot, immunofluorescence, and immunohistochemistry with mPGES-1–specific antibodies.

Results

Western blotting revealed that mPGES-1 expression was significantly elevated in AD tissue. Furthermore, immunofluorescence of mPGES-1 was observed in neurons, microglia, and endothelial cells of control and AD tissue. Although mPGES-1 was consistently present in astrocytes of control tissue, it was present in only some astrocytes of AD tissue. Immunohistochemical staining suggested that mPGES-1 was elevated in pyramidal neurons of AD tissue when compared with controls.

Conclusions

The results suggest that mPGES-1 is normally expressed constitutively in human neurons, microglia, astrocytes, and endothelial cells but is up-regulated in AD.

Keywords: β-Amyloid, Cyclooxygenase, Middle frontal gyrus, Neuroinflammation, PGES

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PII: S1552-5260(07)00636-X

doi:10.1016/j.jalz.2007.10.015

Alzheimer's & Dementia: The Journal of the Alzheimer's Association
Volume 4, Issue 1 , Pages 6-13, January 2008